These Ki-rasG12C transgenic mice express the human KRASG12C mutation under the control of a tetracycline-responsive promoter element (TRE; tetO). When hemizygotes are bred with another transgenic mouse expressing either reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA) under the regulation of tissue-specific promoters, transgene expression in the appropriate tissues of the bitransgenic offspring can be regulated with the tetracycline analog, doxycycline.
Mark S. Miller, Wake Forest Univ, School of MedicineRead More +
Hemizygous mice are viable and fertile. These Ki-rasG12C transgenic mice express the human KRASG12C mutation under the control of a tetracycline-responsive promoter element (TRE; tetO). When hemizygotes are bred with another transgenic mouse expressing either reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA) under the regulation of tissue-specific promoters, transgene expression in the appropriate tissues of the bitransgenic offspring can be regulated with the tetracycline analog, doxycycline.
When crossed with mice containing a lung-specific rtTA protein (e.g. Stock Nos. 006222, 006232, 006242 or 006225), treatment with doxycycline results in the formation of benign hyperplastic lesions starting at 12 weeks and the development of benign adenomas by 6 months. Tumors do not progress in size, but multiplicity increases upon further treatment with doxycyline. These bitransgenic mice live for at least 12 months and show a benign phenotype as compared with other mutant KRAS transgenic strains (e.g. Stock No. 004375), which demonstrate more aggressive tumor phenotypes. Doxycycline withdrawl from the diet of bitransgenic mice results in tumor regression.
A genomic segment including the KRASG12C (Ki-rasG12C) mutation was cloned from the H358 human lung bronchioalveolar cell line and placed under the regulation of a tetracycline-responsive element (TRE; tetO). The transgenic construct was microinjected into fertilized FVB/N mouse eggs. Transgenic founders were crossed with non-transgenic littermates to establish germline transmission.
|Expressed Gene||KRAS, Kirsten rat sarcoma viral oncogene homolog, human|
|Site of Expression|
|Allele Name||transgene insertion 9.1, Mark Miller|
|Allele Type||Transgenic (Humanized sequence, Inducible, Inserted expressed sequence)|
|Gene Symbol and Name||Tg(tetO/CMV-KRAS*G12C)9.1Msmi, transgene insertion 9.1, Mark Miller|
|Promoter||CMV, cytomegalovirus, human|
|Promoter||tetO, tet operator,|
|Expressed Gene||KRAS, Kirsten rat sarcoma viral oncogene homolog, human|
|Strain of Origin||FVB/NTac|
|Molecular Note||A genomic segment including the KRASG12C mutation was cloned from the H358 human lung bronchioalveolar cell line and placed under the regulation of a tetracycline-inducible (tetO)/cytomegalovirus (CMV) promoter. Copy number is estimated at 22.|
|Mutations Made By|| |
Mark Miller, Wake Forest Univ, School of Medicine
|Please inquire about possible genotypes.|
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